Molecular biomedicine最新文献

{"title":"Hyaluronidase: structure, mechanism of action, diseases and therapeutic targets.","authors":"Jiamin Lu, Zheng Zhao, Lingli Pan, Hui Wu, Shibing Wang, Xiangmin Tong, Shenghao Wu","doi":"10.1186/s43556-025-00299-y","DOIUrl":"10.1186/s43556-025-00299-y","url":null,"abstract":"<p><p>Hyaluronidase (HAase), a family of enzymes critical for regulating physiological and pathological states, catalyzes the degradation of hyaluronic acid (HA), a key component of the extracellular matrix (ECM). By modulating ECM composition and cellular signaling pathways, HAase plays a pivotal role in diverse biological processes, including wound healing, tissue regeneration, and tumor progression. This review systematically elucidates the classification, biological sources, structural diversity, and catalytic mechanisms of HAase, emphasizing its dynamic involvement in disease pathogenesis and diagnostic potential. Furthermore, the article explores innovative therapeutic strategies centered on HAase modulation. HAase inhibitors emerge as promising tools for maintaining HA homeostasis, with implications in anti-inflammatory, antimicrobial, and antitumor therapies by blocking excessive HA degradation. Concurrently, HAase-mediated drug delivery systems represent a paradigm shift in overcoming biological barriers, enhancing bioavailability, and optimizing therapeutic outcomes through ECM remodeling. Notably, the synergy between HAase and immunotherapeutic modalities, such as checkpoint inhibitors and adoptive cell therapies, demonstrates synergistic antitumor effects by reshaping the tumor microenvironment (TME) and augmenting immune cell infiltration. Nevertheless, numerous challenges persist in the clinical application of hyaluronidase, including its immunogenicity, safety, application limitations and ethical considerations. This review synthesizes current research advances and unresolved issues, integrating molecular insights with translational perspectives, aiming to provide a more comprehensive and in-depth understanding of hyaluronidase and to advance clinical therapeutic strategies for hyaluronidase.</p>","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"6 1","pages":"50"},"PeriodicalIF":6.3,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12254123/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144621444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA small nucleolar RNA host gene 1 (SNHG1) mediates acidic bile salt-induced EMT via the ULK1-Notch1 axis in Barrett's esophagus.","authors":"Jianfeng Zhou, Rongyan Zhao, Zixiang Li, Xuelan Ma, Wenke Jin, Yong Yuan, Ning Li, Bo Liu, Yushang Yang","doi":"10.1186/s43556-025-00285-4","DOIUrl":"10.1186/s43556-025-00285-4","url":null,"abstract":"<p><p>Barrett's esophagus (BE) is a precancerous condition closely linked to chronic gastroesophageal reflux disease, characterized by the abnormal transformation of esophageal squamous mucosa into specialized intestinal-type epithelium, significantly elevating the risk of esophageal adenocarcinoma (EAC). Recurrent acidic bile reflux promotes epithelial-mesenchymal transition (EMT), a critical event driving malignant progression. However, the underlying molecular mechanisms remain incompletely understood. Here, we identify the long non-coding RNA small nucleolar RNA host gene 1 (SNHG1) as a novel regulator of EMT in BE, mediating its effects through the UNC-52-like kinase 1 (ULK1)-Notch1 signaling axis and autophagy modulation. Using BAR-T and CP-C cell models, we demonstrate that SNHG1 expression is elevated following acidic bile salt exposure, enhancing EMT characteristics by promoting the phosphorylation of ULK1 and activating Notch1 signaling. Pharmacological interventions targeting autophagy (Rapamycin) and Notch signaling (DAPT) further confirmed that SNHG1's effects on EMT are mediated via modulation of the autophagy-Notch1 interplay. We further validated our results in vivo using the previously described IL1β-induced Lgr5-CreERT2; p16^flox/flox/Kras^G12D mouse model, which reliably reproduces the histological progression of Barrett's-like dysplasia in the squamocolumnar junction (SCJ), confirming SNHG1's critical role in regulating EMT and BE progression. Additionally, SNHG1 expression was significantly elevated in patients who progressed to low- or high-grade dysplasia, as confirmed by diagnostic endoscopic biopsies. Collectively, our study uncovers SNHG1 as a central molecular mediator linking acidic bile-induced EMT and autophagy regulation via the ULK1-Notch1 axis, highlighting its potential as a therapeutic target for preventing BE recurrence and progression to EAC.</p>","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"6 1","pages":"49"},"PeriodicalIF":6.3,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12238433/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144593097","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Homeobox protein B6 and homeobox protein B8 control immune-cancer cell interactions in pancreatic cancer.","authors":"Ludivine Bertonnier-Brouty, Sara Bsharat, Kavya Achanta, Jonas Andersson, Thanya Pranomphon, Tania Singh, Tuomas Kaprio, Jaana Hagström, Caj Haglund, Hanna Seppänen, Rashmi B Prasad, Isabella Artner","doi":"10.1186/s43556-025-00292-5","DOIUrl":"10.1186/s43556-025-00292-5","url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC) is a lethal cancer lacking effective drugs and therefore new treatment targets are needed. In this study, we define the role of homeobox protein B6 (HOXB6) and HOXB8 in controlling pancreatic cancer tumorigenesis and immune response. Transcriptomic analysis comparing human embryonic and PDAC tissue identified a large overlap of expression profiles suggesting a re-initiation of developmental programs in pancreatic cancer. Specifically, we identified the transcription factors HOXB6 and HOXB8 as potential regulators in PDAC. We described their functions in pancreatic cancer by performing transcriptomic and tumor tissue microarray analyses, in vitro assays in pancreatic and lung cancer cell lines and co-culture experiments with immune cells. Loss of HOXB6 and HOXB8 in pancreatic cancer cells inhibited cell proliferation, induced apoptosis and senescence and enhanced gemcitabine sensitivity. Moreover, reduced HOXB6 and HOXB8 expression in pancreatic and lung adenocarcinoma cell lines affected transcription of immune response pathways which resulted in an increased sensitivity of cancer cells to anti-tumorigenic activities of macrophages suggesting that the HOXB6 and HOXB8 immune regulatory function is conserved in different cancer types. Additionally, naïve M0 macrophages exposed to HOXB8 deficient PDAC cells were unable to differentiate into tumor-associated macrophages, suggesting that HOXB8 promotes the transition of initial anti-tumor macrophage to a tumor-promoting macrophage phenotype in pancreatic cancer. Our findings indicate that HOXB6 and HOXB8 play important roles in regulating cell proliferation, immune response, and treatment resistance to promote pancreatic cancer tumorigenesis and could be useful therapeutic targets.</p>","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"6 1","pages":"48"},"PeriodicalIF":6.3,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12229978/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144577178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel viroid-like RNA element \"Obelisks\": a major breakthrough in the RNA World.","authors":"Li Li, Xinqin Zhang, Min Wu","doi":"10.1186/s43556-025-00290-7","DOIUrl":"10.1186/s43556-025-00290-7","url":null,"abstract":"","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"6 1","pages":"47"},"PeriodicalIF":6.3,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12226432/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144562201","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emerging role of N-acetyltransferase 10 in diseases: RNA ac4C modification and beyond.","authors":"Lin Jiao, Yanjun Si, Yushan Yuan, Xinxing Lei, Qian Jiang, Lijun Yang, Wenhao Mao, Binwu Ying, Liwei Ma, Ting Sun","doi":"10.1186/s43556-025-00286-3","DOIUrl":"10.1186/s43556-025-00286-3","url":null,"abstract":"<p><p>N⁴-acetylcytidine (ac4C), a conserved RNA modification, plays critical roles in RNA stability and translation. As the primary enzyme catalyzing ac4C, N-acetyltransferase 10 (NAT10) is increasingly implicated in diverse diseases. This review systematically explores NAT10's multifaceted contributions to cancer, autoimmune disorders, infectious diseases, cardiovascular conditions, and metabolic syndromes. In cancer, NAT10 drives malignancy by enhancing oncogenic processes such as proliferation, metastasis, and therapy resistance, with overexpression linked to poor prognosis across multiple malignancies. Beyond oncology, NAT10 dysregulation is associated with autoimmune diseases like rheumatoid arthritis and systemic lupus erythematosus, where it modulates immune responses through RNA acetylation. In infectious contexts, NAT10 influences sepsis progression and viral pathogenesis by stabilizing pathogen-related RNAs, while in cardiovascular diseases, it exacerbates myocardial injury and heart failure through ac4C-dependent and independent pathways. Additionally, NAT10 promotes metabolic dysfunction-associated steatotic liver disease by regulating lipid metabolism genes. The review further discusses therapeutic strategies targeting NAT10, including small-molecule inhibitors and gene silencing approaches, which show promise in preclinical models by suppressing tumor growth, enhancing chemosensitivity, and mitigating inflammatory damage. By integrating molecular insights and clinical relevance, this work underscores NAT10 as a pivotal regulator of disease mechanisms and a potential target for future therapeutic interventions. Future research should address context-dependent roles, refine ac4C detection methods, and explore combinatorial therapies to overcome resistance mechanisms.</p>","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"6 1","pages":"46"},"PeriodicalIF":6.3,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12209103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144531460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cancer pain: molecular mechanisms and management.","authors":"Wan-Li Wang, Yi-Hang Hao, Xin Pang, Ya-Ling Tang","doi":"10.1186/s43556-025-00289-0","DOIUrl":"10.1186/s43556-025-00289-0","url":null,"abstract":"<p><p>Cancer pain, a highly prevalent and distressing symptom among cancer patients, has a seriously harmful effect on their life and presents a complex challenge in clinical management. Despite extensive research efforts and the existence of clinical guidelines, significant controversies persist regarding the molecular mechanisms underpinning cancer pain as well as the most effective management strategies. This review systematically delves into the neurobiological underpinnings of cancer pain, centering on the interplay of peripheral and central sensitization, cellular stress and dysfunction, as well as the crucial roles of various signaling pathways and epigenetic regulation in its pathogenesis. In terms of treatment, the fundamental strategy involves a comprehensive initial assessment of cancer pain, followed by targeted interventions based on the assessment findings. It advocates for a multimodal approach that integrates pharmacological with non-pharmacological therapies. However, ongoing debates surround issues related to opioid rotation protocols and the long-term safety of opioid use. Furthermore, it underscores the underexplored potential of personalized therapies targeting molecular pathways and the need for standardized, interdisciplinary pain assessment tools. By bridging mechanistic research and clinical practice, this work potentially provides a framework for refining guideline implementation, advancing targeted therapies, and improving patient-centered care, thereby contributing to the evolution of precision oncology and holistic pain management paradigms.</p>","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"6 1","pages":"45"},"PeriodicalIF":6.3,"publicationDate":"2025-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12205135/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144512904","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Leucine-rich pentatricopeptide repeat-containing protein (LRPPRC)-stabilized lncRNA small nucleolar RNA host gene 15 (Snhg15) modulates hematopoietic injury induced by γ-ray irradiation via m⁶A modification.","authors":"Shuqin Zhang, Yajia Cheng, Yujia Gao, Feifei Xu, Yuna Wang, Junling Zhang, Yue Shang, Deguan Li, Saijun Fan","doi":"10.1186/s43556-025-00279-2","DOIUrl":"10.1186/s43556-025-00279-2","url":null,"abstract":"<p><p>With advancements in radiotherapy technologies, the detrimental effects of ionizing radiation on biological systems, particularly the hematopoietic system, have caused significant concern. N⁶-methyladenosine (m⁶A), the most pervasive representative of post-transcriptional modifications, plays critical roles in diverse biological events. Non-coding RNA comprises the vast majority of the human genome. This study aimed to explore the role of long non-coding RNA (lncRNA) m⁶A modification in γ-ray irradiation-induced hematopoietic injury. By using mouse models, it was found that γ-radiation rapidly damaged hematopoietic bone marrow cells (BMCs), triggering apoptosis, oxidative stress and DNA damage, along with up-regulation of m⁶A Reader proteins. We revealed the time-conditioned landscape of lncRNA m⁶A methylome of BMCs in the short term after radiation and found that a dynamic \"change-then-recover\" trend involved. LncRNA Snhg15 was identified as a key regulator through integration analysis of the methylome and transcriptome data. Its m⁶A modification was closely related to progression of radiation injury in BMCs. Further research demonstrated that the novel m⁶A Reader LRPPRC could interact with the modification site of Snhg15, stabilize Snhg15 and promote its expression, thereby exacerbating radiation-induced injury to BMCs both in vitro and in vivo. Knockdown of Lrpprc or Snhg15 could alleviate the radiation injury to the hematopoietic system. Additionally, the LRPPRC-Snhg15 axis was involved in the radio-protective efficacy of gut microbiota-derived valeric acid. These findings uncover a novel mechanism by which m⁶A-modified lncRNA Snhg15 is stabilized by LRPPRC modulates γ-irradiation-induced hematopoietic injury, providing potential therapeutic targets for the prevention and treatment of radiation injuries.</p>","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"6 1","pages":"44"},"PeriodicalIF":6.3,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12187624/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144487460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fructose metabolism and its roles in metabolic diseases, inflammatory diseases, and cancer.","authors":"Zhenhong Li, Xinzou Fan, Fan Gao, Shengguang Pan, Xiao Ma, Hao Cheng, Hiroko Nakatsukasa, Wei Zhang, Dunfang Zhang","doi":"10.1186/s43556-025-00287-2","DOIUrl":"10.1186/s43556-025-00287-2","url":null,"abstract":"<p><p>Fructose, a prevalent hexose, has become a widely used food additive, with its usage rising significantly because of socio-economic advancements and shifts in human dietary habits. Excessive fructose intake has been implicated in obesity, cardiovascular disease, metabolic syndromes, inflammation, and cancer, among other disorders. This review discusses the absorption, distribution, and metabolism of fructose and the links between fructose metabolism and major metabolic pathways. The role of fructose in metabolic diseases, including metabolic dysfunction-associated fatty liver disease, hyperinsulinemia, and hyperuricemia, is also highlighted. Furthermore, the role of fructose in the development of chronic inflammation, including gut inflammation, liver inflammation, and neuroinflammation, is discussed. Lastly, in the context of cancer development, this review summarizes the dual role of fructose in tumors, both pro- and anti-tumor effects. Future studies on the role of fructose in cancer should focus on the complexity of physiological and pathological conditions, such as the specific tumor microenvironment and metabolic status. Fructose has been shown to induce metabolic reprogramming of multiple immune cells and increase pro-inflammatory immune responses; therefore, inhibiting or promoting its metabolism may regulate immune responses. And targeting fructose metabolism may be a promising approach to treating metabolic diseases, inflammation, and cancer.</p>","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"6 1","pages":"43"},"PeriodicalIF":6.3,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12185857/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144478145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of mitochondria in physiological activities, diseases, and therapy.","authors":"Lilin Wang, Xiaoting Zhou, Tianqi Lu","doi":"10.1186/s43556-025-00284-5","DOIUrl":"10.1186/s43556-025-00284-5","url":null,"abstract":"<p><p>Mitochondria are generally considered essential for life in eukaryotic organisms because they produce most of the energy or adenosine triphosphate (ATP) needed by the cell. Beyond energy production, it is now widely accepted that mitochondria also play a pivotal role in maintaining cellular homeostasis and signaling. The two core processes of mitochondrial dynamics, fission and fusion, serve as crucial foundations for maintaining mitochondrial morphology, distribution, and quantity, thereby ensuring cellular homeostasis. Mitochondrial autophagy (mitophagy) ensures the selective degradation of damaged mitochondria, maintaining quality control. Mitochondrial transport and communication further enhance their role in cellular processes. In addition, mitochondria are susceptible to damage, resulting in dysfunction and disruption of intracellular homeostasis, which is closely associated with the development of numerous diseases. These include mitochondrial diseases, neurodegenerative diseases, cardiovascular diseases (CVDs) and stroke, metabolic disorders such as diabetes mellitus, cancer, infectious diseases, and the aging process. Given the central role of mitochondria in disease pathology, there is a growing need to understand their mechanisms and develop targeted therapies. This review aims to provide a comprehensive overview of mitochondrial structure and functions, with a particular focus on their roles in disease development and the current therapeutic strategies targeting mitochondria. These strategies include mitochondrial-targeted antioxidants, modulation of mitochondrial dynamics and quality control, mitochondrial genome editing and genetic therapy, and mitochondrial transplantation. We also discuss the challenges currently facing mitochondrial research and highlight potential future directions for development. By summarizing the latest advancements and addressing gaps in knowledge, this review seeks to guide future research and clinical efforts in the field of mitochondrial medicine.</p>","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"6 1","pages":"42"},"PeriodicalIF":6.3,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12179052/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144328011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosomes in inflammation and cancer: from bench to bedside applications.","authors":"Shiyuan Huang, Fang Yan, Yi Qiu, Tao Liu, Wenjin Zhang, Yige Yang, Rao Zhong, Yang Yang, Xi Peng","doi":"10.1186/s43556-025-00280-9","DOIUrl":"10.1186/s43556-025-00280-9","url":null,"abstract":"<p><p>Exosomes, lipid bilayer nanovesicles secreted by nearly all cell types, play pivotal roles in intercellular communication by transferring proteins, nucleic acids, and lipids. This review comprehensively summarizes their multiple functions in inflammation and cancer. In inflammation, exosomes exhibit context-dependent pro- or anti-inflammatory effects: they promote acute responses by delivering cytokines and miRNAs to activate immune cells, yet suppress chronic inflammation via immunoregulatory molecules. Two representative inflammatory diseases, namely sepsis and inflammatory bowel disease, were highlighted to elucidate their roles in the acute and chronic inflammatory diseases. In cancer, exosomes orchestrate tumor microenvironment (TME) remodeling by facilitating angiogenesis, metastasis, and immune evasion through interactions with cancer-associated fibroblasts, tumor-associated macrophages, and extracellular matrix components. Furthermore, exosomes can facilitate the transition from inflammation to cancer by impacting pertinent signaling pathways via their transported oncogenic and inflammatory molecules. Tumor-derived exosomes also serve as non-invasive biomarkers correlating with disease progression. Clinically, exosomes demonstrate promise as therapeutic agents and drug carriers, evidenced by ongoing trials targeting inflammatory diseases and cancers. However, challenges in isolation standardization, scalable production, and understanding functional heterogeneity hinder clinical translation. Future research should prioritize elucidating cargo-specific mechanisms, optimizing engineering strategies, and advancing personalized exosome-based therapies. By bridging molecular insights with clinical applications, exosomes hold great potential in precision medicine for inflammation and oncology.</p>","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"6 1","pages":"41"},"PeriodicalIF":6.3,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12149089/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144259519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}